ArticleBMC psychiatry2025
Association of prenatal alcohol exposure and prenatal depressive symptoms with offspring hair cortisol in childhood and adolescence.
Article in BMC psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Perinatal HPA axis regulation and offspring neuropsychiatric development: mechanisms, developmental trajectories, and clinical implications.Frontiers in endocrinology · 2026Review
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12 authors.
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Abstract
backgroundPrenatal alcohol exposure (PAE) and maternal depressive symptoms are associated with hypothalamic-pituitary-adrenal (HPA) axis alterations in the offspring. The present study investigated long-term associations of both risk factors on the offspring’s hair cortisol concentration (HCC) in childhood and adolescence.
methodsThe HCC of n = 94 children was assessed at primary school age (T1, M = 7.7 years, SD = 0.81) and in early adolescence (T2, M = 13.3 years, SD = 0.30). PAE was operationalized by maternal self-report and the meconium alcohol metabolite ethyl glucuronide (EtG), applying two cut-off values, EtG ≥ 10 ng/g (EtG10+: n = 18) and EtG ≥ 154 ng/g (EtG154+: n = 9). The Edinburgh Postnatal Depression Scale (EPDS) was used to screen for prenatal maternal depressive symptoms (EPDS ≥ 10: n = 24). The clinical relevance of the results was assessed by correlating the HCC with children’s emotional and behavioral problems as measured by the Strengths and Difficulties Questionnaire (SDQ).
resultsThe EtG10+ and the EtG154+ group showed lower HCC at T1 than the respective control groups, with a significant difference observed for the EtG154 risk group (p = .032). This difference was attenuated at T2. Children and adolescents whose mothers reported prenatal depressive symptoms did not show any significant differences in HCC at any time.
conclusionThe present study provides further evidence of long-term effects of alcohol consumption during pregnancy on the HPA axis development of the child, as manifested in distinct trajectories of HCC from primary school age to early adolescence. CLINICAL TRIAL NUMBER: Not applicable.
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